Bhaumik S, Anjum R, Rangaraj N, Pardhasaradhi B V, Khar A
Centre for Cellular and Molecular Biology, Hyderabad, India.
FEBS Lett. 1999 Aug 6;456(2):311-4. doi: 10.1016/s0014-5793(99)00969-2.
Curcumin, the active ingredient of the rhizome of Curcuma longa has anti-inflammatory, antioxidant and antiproliferative activities. Although its precise mode of action remains elusive, studies have shown that chemopreventive action of curcumin might be due to its ability to induce apoptosis in cancer cells. Curcumin was shown to be responsible for the inhibition of AK-5 tumor (a rat histiocytoma) growth by inducing apoptosis in AK-5 tumor cells via caspase activation. This study was designed to investigate the mechanism leading to the induction of apoptosis in AK-5 tumor cells. Curcumin treatment resulted in the hyperproduction of reactive oxygen species (ROS), loss of mitochondrial membrane potential (delta psi(m)) and cytochrome c release to the cytosol, with the concomitant exposure of phosphatidylserine (PS) residues on the cell surface. This study suggests redox signalling and caspase activation as the mechanisms responsible for the induction of curcumin mediated apoptosis in AK-5 tumor cells.
姜黄素是姜黄根茎的活性成分，具有抗炎、抗氧化和抗增殖活性。尽管其确切作用方式尚不清楚，但研究表明，姜黄素的化学预防作用可能归因于其诱导癌细胞凋亡的能力。研究显示，姜黄素通过激活半胱天冬酶诱导AK-5肿瘤细胞（一种大鼠组织细胞瘤）凋亡，从而抑制AK-5肿瘤生长。本研究旨在探究导致AK-5肿瘤细胞凋亡诱导的机制。姜黄素处理导致活性氧（ROS）过度产生、线粒体膜电位（Δψm）丧失以及细胞色素c释放到细胞质中，同时细胞表面磷脂酰丝氨酸（PS）残基暴露。本研究表明，氧化还原信号传导和半胱天冬酶激活是姜黄素介导AK-5肿瘤细胞凋亡诱导的机制。
